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The decline of NAD + with age results from three converging factors: (1) increased activity of CD38, a NADase whose expression increases with age-related chronic inflammation (inflammaging), (2) reduced biosynthesis via the NAMPT (nicotinamide phosphoribosyltransferase) and NMN pathways, and (3) increased demand for NAD+ by PARP-1 to repair increasing oxidative DNA damage

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[1] These GLP-1 agonist medications bind to GLP-1 receptors to trigger the effects of the GLP-1 hormone